The objective of the proposed research is to determine the physiological significance and pathophysiological implications of the autonomic nervous control of cerebral circulation. In previous studies the applicant has demonstrated that direct electrical stimulation of the sympathetic innervation of the cerebral vessels is capable of producing marked decrease in cerebral blood flow in the anesthetized dog. In as much as the brain is the target organ of anesthesia, and the effect of anesthesia on cerebral blood flow and metabolism is not completely understood, a chronic unanesthetized preparation for the continuous moment to moment measurement of cerebral blood flow will be used to examine the physiological significance of this sympathetic control mechanism. It will be determined if the cerebral vasculature is involved in the cardiovascular reflex adjustments to a variety of stresses including normotensive hemorrhage, exercise and temperature. A cerebral venous outflow technique using a Doppler ultrasonic flow transducer on an intraboney cerebral venous sinus has been developed and used in pilot studies. The preparation is free from extracerebral contamination from the face, muscle masses and skin and does not involve damage to sympathetic nerves that could be encountered in arterial flow measurements. Autonomic agonists and antagonists will be used to mimic or block reflex changes in cerebral blood flow. The possibility of denervation supersensitivity to autonomic agonists will be evaluated in chronically sympathectomized dogs. Acute studies on parasympathetic control and regional distribution of radioactive microspheres in the cerebral circulation will complement the chronic studies in unanesthetized dogs.